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https://www.selleckchem.com/products/hydroxychloroquine-sulfate.html The deposition of amyloid-beta (Aβ) through the cleavage of amyloid-beta precursor protein (APP) is a biomarker of Alzheimer's disease (AD). This study used QIAGEN Ingenuity Pathway Analysis (IPA) to conduct meta-analysis on the molecular mechanisms by which methamphetamine (METH) impacts AD through modulating the expression of APP. All the molecules affected by METH and APP were collected from the QIAGEN Knowledge Base (QKB); 78 overlapping molecules were identified. Upon simulation of METH exposure using the "Molecule Activity Predictor" feature, eight molecules were found to be affected by METH and exhibited activation relationships on APP expression at a confidence of p = 0.000453 (Z-score = 3.51, two-tailed). Core Analysis of these eight molecules identified High Mobility Group Box protein 1 (HMGB1) signaling pathway among the top 5 canonical pathways with most overlap with the 8-molecule dataset. Simulated METH exposure increased APP expression through HMGB1 at a confidence of p less then 0.00001 (Z-score = 7.64, two-tailed). HMGB1 is a pathogenic hallmark in AD progression. It not only increases the production of inflammatory mediators, but also mediates the disruptionof the blood-brain barrier. Our analyses suggest the involvement of HMGB1 signaling pathway in METH-induced modulation of APP as a potential casual factor of AD.Colon cancer remains one of the leading causes of cancer-related deaths worldwide. Transformation of colon epithelial cells into invasive adenocarcinomas has been well known to be due to the accumulation of multiple genetic and epigenetic changes. In the past decade, the etiology of inflammatory bowel disease (IBD) which is characterized by chronic inflammation of the intestinal mucosa, was only partially explained by genetic studies providing susceptibility loci, but recently epigenetic studies have provided critical evidences affecting IBD pathogenesis. Over the past

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